Effect of ions & hormones on Cardiac muscle

1. Effect Of Ions And Hormones
On Cardiac Muscle
Dr. Sara Sadiq

2. Ions that act over Heart
• Sodium
• Calcium
• Potassium

3. Action Potentials in Cardiac Muscle
Figure 20–15

4. Pacemaker cells

5. Calcium Ion Contraction
• Contraction of a cardiac muscle cell is produced by an
increase in calcium ion concentration around myofibrils
 20% of calcium ions required for a contraction enter cell
membrane through slow channels during plateau phase
 This extracellular Ca2+ triggers release of calcium ion
reserves from sarcoplasmic reticulum (80%)
This is why heart is so sensitive to blood calcium

6. Ionic imbalances
Potassium
• Decreases K+ gradient, inhibits
repolarization => -ve chronotropic effect
• Increases K+ gradient, causes
hyperpolarization of resting membranes =>
+ve chronotropic effect

7. Ionic imbalances
Calcium
• Hypercalcemia: cardiac muscle
cells become very excitable => +ve
ionotropic effect
• Hypocalcemia: decrease
excitability => -ve ionotropic
effect

8. Chemoreceptor Reflex
- stimulated by oxygen, pH, or CO2
- overall effect: positive chronotropic and inotropic.

10. Hormonal Effects on Cardiac Muscle
• Epinephrine (E)
• Norepinephrine (NE)
• Thyroid hormone

11. • Epinephrine:
• released from adrenal gland.
• Stimulated by ANS.
• Norepinephrine:
No direct cardiac stimulation

12. Figure 20–21 (Navigator)
Autonomic NS
Innervation
• Heart is stimulated
by the sympathetic
cardio acceleratory
center
• Heart is inhibited
by the
parasympathetic
cardio inhibitory
center

13. Sympathetic Nervous System
- Controls all components of the heart.
- Release Norepinephrine (NE).
- Act through β1 receptor.
Cell
1

14. Norepinephrine:
- +ve chronotropic
- +ve inotropic.
How?
 spontaneous depolarization of SA- node.
■  permeability to K+  less K+ efflux.
■  permeability to Ca2+  more Ca2+ influx.
■ As a result, the slope of depolarization , causing  rate of SA- node firing
&  HR.

15. Cell
m
Parasympathetic Nervous System (PNS)
- controls SA node and AV node.
- releases Acetylcholine (Ach).
- Act through Muscarinic receptor

16. Accetylcholine:
• -ve ionotropic (prolongs delay at AV node).
• -ve chronotropic.
How?
 spontaneous depolarization of SA- node.
■  SA- node membrane permeability to K+  more K+ efflux.
■  membrane permeability to Ca2+  less Ca2+ influx.
■ As a result, the prepotential slope , causing  rate of SA- node firing & 
HR.

19. • Thyroxin:
• released from thyroid
gland.
• increases heart rate.

20. THANKYOU